Scientists from St. Louis University School of Medicine (SLUSM) headed by Dr. Thomas Burris, Chair of pharmacological and physiological science have reported that their team has found a way to prevent type I diabetes in an animal model. Their findings was published in the journal Endocrinology. Type 1 Diabetes is a chronic autoimmune disease, meaning the body considers its own pancreatic beta cells as ‘foreign’ and destroys it, resulting in insulin deficiency and causes hyperglycaemia. Treatment for type 1 diabetes involves insulin therapy to control blood sugar and must be continued throughout one’s life. Hence, the team focussed on blocking this autoimmune process, aiming to develop therapies to prevent the illness from developing rather than treating its symptoms.
Previous studies have described in depth about the two types of “T cells” which contribute to the development of type 1 diabetes, namely CD8+ T cells and TH1 cells. However, the role of a third type -TH17 cells in the onset of diabetes was unclear till now. In this study, the team focused on blocking two nuclear receptors, retinoic acid receptor-related-orphan receptors (RORα and RORγt) that play a critical role in the development of TH17 cells. By blocking these receptors with a substance called SR1001(a selective RORα/γ inverse agonist developed by Burris), none of the treated mice developed diabetes compared with more than 70% of mice in the control group which did not receive SR1001. They were able to prevent the destruction of beta cells which are responsible for producing insulin.
“None of the animals on the treatment developed diabetes even when we started treatment after significant beta cell damage had already occurred. We believe this type of treatment would slow the progression of type I diabetes in people or potentially even eliminate the need for insulin therapy,” said Burris. Since, TH17 has been confirmed to play a key role in the development of type 1 diabetes, drugs which target these cell types may offer new avenues for the treatment of type 1 diabetes.
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